Pyloric stenosis of Infancy, primary hyperacidity and Occam's razor.

An account is given of the process by which the Primary Hyperacidity pathogenesis of Pyloric Stenosis of Infancy (PS) evolved. The initial discovery that fasting gastrins were high at birth and continued to rise within the first 4 days was the starting point. Since acidity was also rising at the same time it was proposed that the usual negative feed-back between gastrin and stomach acidity was not mature in the first few weeks of life. The gastrin model for producing PS in puppy dogs was a further incentive to believe that relatively high gastrins, and secondary high acidity would thereby repeatedly cause sphincter contraction and lead to hypertrophy. When gastrin was found to be normal in PS babies we considered and accepted, the less complicated hypothesis that a Primary Inherited Hyperacidity itself was the driving force. Such a theory explained nearly all the clinical features. When we further considered the expected consequences of an initially ineffective negative feed -back and its later maturation, the known peak acidity in neonatal development was explained. This phenomenon also provided an explanation for the remaining previously unexplained time sensitive features of the condition.

The true cause of pyloric stenosis is hyperacidity.

UNLABELLED: Pyloric stenosis (PS) has no known cause. A testable theory of cause is proposed, based on the inheritance of a parietal cell mass (PCM) at the upper end of the normal range. It is proposed that, until 3-4 wk of age, the obligatory high fasting gastrins are at maximal levels and not able to be diminished by increasing antral acidity. Hence, rising acidity is not reduced by a lowered gastrin during this time, and very high acidity occurs. CONCLUSION: Persisting duodenal hyperacidity is created by an inherited high PCM and loss of gastrin control. These two factors produce pyloric stenosis through work hypertrophy from repeated pyloric contraction in response to hyperacidity.